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Hepatic encephalopathy: from pathophysiology to therapeutic management Volume 20, issue 3, Juillet-Août-Septembre 2014

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Authors
Hôpital Saint-Eloi, département d’hépatogastroentérologie, 80 avenue Augustin Fliche 34295 Montpellier Cedex 5, France
* Tirés à part

Hepatic encephalopathy (HE) is a serious complication of acute and chronic liver disease, characterized by multiple neuropsychiatric symptoms of varying severity. Several pathophysiological hypotheses have been proposed over the last decades, none of which are entirely satisfactory due to the complexity of the mechanisms underlying HE, which involve multiple factors. Nevertheless, a consensus has emerged concerning the central role of ammonia in the pathogenesis of HE, although inflammation and abnormalities in neurotransmission are also involved. Cerebral edema may represent the pathogenic endpoint common to the multiple pathophysiological mechanisms involved in HE. The occurrence of an episode of HE is associated with a poor prognosis in patients with liver disease: in acute liver failure, HE plays a predominant role in deciding whether the patient is a candidate for liver transplantation; in chronic liver failure, HE is considered a turning point in the natural history of the disease. The identification and treatment of precipitating factors is crucial in the management of patients with HE and often allows for a spectacular regression of symptoms. Current therapeutic strategies are aimed at decreasing ammonia production through agents such as non absorbable disaccharides or antibiotics. Finally, in cirrhotic patients with chronic or recurrent HE, liver transplantation remains the ultimate option.